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Blood, 15 July 2001, Vol. 98, No. 2, pp. 475-477
BRIEF REPORT
The human erythropoietin receptor gene rescues erythropoiesis and
developmental defects in the erythropoietin receptor null
mouse
Xiaobing Yu,
Chyuan-Sheng Lin,
Frank Costantini, and
Constance Tom Noguchi
From the Laboratory of Chemical Biology, National
Institute of Diabetes and Digestive and Kidney Disorders,
National Institutes of Health, Bethesda, MD; and the Department of
Genetics and Development, Columbia University, New York, NY.
Erythropoietin and its receptor are required for definitive
erythropoiesis and maturation of erythroid progenitor cells. Mice lacking the erythropoietin receptor exhibit severe anemia and die at
about embryonic day 13.5. This phenotype can be rescued by the human
erythropoietin receptor transgene. Animals expressing only the human
erythropoietin receptor survived through adulthood with normal
hematologic parameters and appeared to respond appropriately to induced
anemic stress. In addition to restoration of erythropoiesis during
development, the cardiac defect associated with embryos lacking
the erythropoietin receptor was corrected and the increased apoptosis
in fetal liver, heart, and brain in the erythropoietin receptor null
phenotype was markedly reduced. These studies indicate that no species
barrier exists between mouse and human erythropoietin receptor and that
the human erythropoietin receptor transgene is able to provide specific
expression in hematopoietic and other selected tissues to rescue
erythropoiesis and other organ defects observed in the erythropoietin
receptor null mouse.
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Related Letter in Blood Online:
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Mouse surviving solely on human erythropoietin receptor (EpoR): model of human EpoR-linked disease
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